Yes / The realisation that unregulated activation of the Janus kinase–signal transducer and activator of transcription (JAK–STAT) pathway is a key driver of a wide range of diseases has identified its components as targets for therapeutic intervention by small molecule inhibitors and biologicals. In this review, we discuss JAK-STAT signalling pathway inhibition by the inducible inhibitor “suppressor of cytokine signaling 3 (SOCS3), its role in diseases such as myeloproliferative disorders, and its function as part of a multi-subunit E3 ubiquitin ligase complex. In addition, we highlight potential applications of these insights into SOCS3-based therapeutic strategies for management of conditions such as vascular re-stenosis associated with acute vascular injury, where there is strong evidence that multiple processes involved in disease progression could be attenuated by localized potentiation of SOCS3 expression levels. / British Heart Foundation; Chief Scientist's Office; NHS Greater Glasgow and Clyde Research Endowment Fund; BBSRC
| Identifer | oai:union.ndltd.org:BRADFORD/oai:bradscholars.brad.ac.uk:10454/7925 |
| Date | 04 May 2014 |
| Creators | Williams, Jamie J.L., Munro, K.M.A., Palmer, Timothy M. |
| Source Sets | Bradford Scholars |
| Language | English |
| Detected Language | English |
| Type | Article, published version paper |
| Rights | (c) 2014 The Authors. Full-text reproduced in accordance with the publisher's self-archiving policy. This work is licensed under a Creative Commons Attribution 4.0 International License. http://creativecommons.org/licenses/by/4.0/ |
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